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AV junctional rhythm induced by sympathetic-parasympathetic imbalance in dog hearts.

作者信息

Furukawa Y, Martin P, Levy M N

机构信息

Department of Investigative Medicine, Mt. Sinai Medical Center, Cleveland, Ohio 44106.

出版信息

Am J Physiol. 1990 Sep;259(3 Pt 2):H839-42. doi: 10.1152/ajpheart.1990.259.3.H839.

DOI:10.1152/ajpheart.1990.259.3.H839
PMID:2396692
Abstract

We studied the atrioventricular (AV) junctional rhythm induced by stimulation of discrete autonomic nerves to the AV nodal area in spontaneously beating hearts of anesthetized dogs where all central autonomic connections to the heart had been cut. Simultaneous stimulation of intracardiac sympathetic and parasympathetic nerves to the AV nodal area (AVSP stimulation, at the junction of the inferior vena cava and left atrium) initially increased and then decreased the AV interval. During such stimuli no AV junctional rhythm was observed; however, after cessation of stimulation, an AV junctional rhythm then appeared in 6 of 12 dogs. Because norepinephrine (NE) persists much longer than acetylcholine in cardiac tissues, we postulated that the junctional rhythm was ascribable to the residual NE that had been released during stimulation. After the animals had been given atropine, an AV junctional rhythm was induced in all animals during AVSP stimulation. These junctional rhythms were suppressed by propranolol or by pacing the atria at a rate faster than the rate of the junctional rhythm. These results suggest that a regional sympathetic-parasympathetic imbalance may unmask subsidiary pacemaking activity, such as an AV junctional rhythm.

摘要

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